Tinea corporis is caused by a tiny fungus known as dermatophyte. These tiny organisms normally live on the superficial skin surface, and when the opportunity is right, they can induce a rash or infection.

The disease can also be acquired by person-to-person transfer usually via direct skin contact with an infected individual. Animal-to-human transmission is also common. Ringworm commonly occurs on pets (dogs, cats) and the fungus can be acquired while petting or grooming an animal. Ringworm can also be acquired from other animals such as horses, pigs, ferrets and cows. The fungus can also be spread by touching inanimate objects like personal care products, bed linen, combs, athletic gear, or hair brushes contaminated by an affected person.

Individuals at high risk of acquiring ringworm include those who:

- Live in crowded, humid conditions.

- Sweat excessively, as sweat can produce a humid wet environment where the pathogenic fungi can thrive. This is most common in the armpits, groin creases and skin folds of the abdomen.

- Participate in close contact sports like soccer, rugby, or wrestling.

- Wear tight, constrictive clothing with poor aeration.

- Have a weakened immune system (e.g., those infected with HIV or taking immunosuppressive drugs).

Advice often given includes:

- Avoid sharing clothing, sports equipment, towels, or sheets.

- Wash clothes in hot water with fungicidal soap after suspected exposure to ringworm.

- Avoid walking barefoot; instead wear appropriate protective shoes in locker rooms and sandals at the beach.

- Avoid touching pets with bald spots, as they are often carriers of the fungus.

Because fungi prefer warm, moist environments, preventing ringworm involves keeping skin dry and avoiding contact with infectious material. Basic prevention measures include:

- Washing hands after handling animals, soil, and plants.

- Avoiding touching characteristic lesions on other people.

- Wearing loose-fitting clothing.

- Practicing good hygiene when participating in sports that involve physical contact with other people.

Tinea capitis caused by species of "Microsporum" and "Trichophyton" is a contagious disease that is endemic in many countries. Affecting primarily pre-pubertal children between 6 and 10 years, it is more common in males than females; rarely does the disease persist past age sixteen. Because spread is thought to occur through direct contact with afflicted individuals, large outbreaks have been known to occur in schools and other places where children are in close quarters; however, indirect spread through contamination with infected objects ("fomites") may also be a factor in the spread of infection. In the USA, tinea capitis is thought to occur in 3-8% of the pediatric population; up to one-third of households with contact with an infected person may harbor the disease without showing any symptoms.

The fungal species responsible for causing tinea capitis vary according to the geographical region, and may also change over time. For example, "Microsporum audouinii" was the predominant etiological agent in North America and Europe until the 1950s, but now "Trichophyton tonsurans" is more common in the USA, and becoming more common in Europe and the United Kingdom. This shift is thought to be due to the widespread use of griseofulvin, which is more effective against "M. audounii" than "T. tonsurans"; also, changes in immigration patterns and increases in international travel have likely spread "T. tonsurans" to new areas. Another fungal species that has increased in prevalence is "Trichophyton violaceum", especially in urban populations of the United Kingdom and Europe.

no approved human vaccine exist against "Dermatophytosis". For horses, dogs and cats there is available an approved inactivated vaccine called "Insol Dermatophyton" (Boehringer Ingelheim) which provides time-limited protection against several trichophyton and microsporum fungal strains.

According to the National Health Service, "Athlete’s foot is very contagious and can be spread through direct and indirect contact." The disease may spread to others directly when they touch the infection. People can contract the disease indirectly by coming into contact with contaminated items (clothes, towels, etc.) or surfaces (such as bathroom, shower, or locker room floors). The fungi that cause athlete's foot can easily spread to one's environment. Fungi rub off of fingers and bare feet, but also travel on the dead skin cells that continually fall off the body. Athlete's foot fungi and infested skin particles and flakes may spread to socks, shoes, clothes, to other people, pets (via petting), bed sheets, bathtubs, showers, sinks, counters, towels, rugs, floors, and carpets.

When the fungus has spread to pets, it can subsequently spread to the hands and fingers of people who pet them. If a pet frequently gnaws upon itself, it might not be fleas it is reacting to, it may be the insatiable itch of tinea.

One way to contract athlete's foot is to get a fungal infection somewhere else on the body first. The fungi causing athlete's foot may spread from other areas of the body to the feet, usually by touching or scratching the affected area, thereby getting the fungus on the fingers, and then touching or scratching the feet. While the fungus remains the same, the name of the condition changes based on where on the body the infection is located. For example, the infection is known as tinea corporis ("ringworm") when the torso or limbs are affected or tinea cruris (jock itch or dhobi itch) when the groin is affected. Clothes (or shoes), body heat, and sweat can keep the skin warm and moist, just the environment the fungus needs to thrive.

Globally, fungal infections affect about 15% of the population and affects one out of five adults. Athlete's foot is common in individuals who wear occlusive shoes. Countries and regions where going barefoot is more common experience much lower rates of athlete's foot than do populations which habitually wear shoes; as a result, the disease has been called "a penalty of civilization". Studies have demonstrated that men are infected 2–4 times more often than women.

It may appear as thickened, scaly, and sometimes boggy swellings, or as expanding raised red rings (ringworm). Common symptoms are severe itching of the scalp, dandruff, and bald patches where the fungus has rooted itself in the skin. It often presents identically to dandruff or seborrheic dermatitis. The highest incidence in the United States of America is in American boys of school age.

There are three type of tinea capitis, microsporosis, trichophytosis, and favus; these are based on the causative microorganism, and the nature of the symptoms. In "microsporosis", the lesion is a small red papule around a hair shaft that later becomes scaly; eventually the hairs break off 1–3 mm above the scalp. This disease used to be caused primarily by "Microsporum audouinii", but in Europe, "M. canis" is more frequently the causative fungus. The source of this fungus is typically sick cats and kittens; it may be spread through person to person contact, or by sharing contaminated brushes and combs. In the United States, "Trichophytosis" is usually caused by "Trichophyton tonsurans", while "T. violaceum" is more common in Eastern Europe, Africa, and India. This fungus causes dry, non-inflammatory patches that tend to be angular in shape. When the hairs break off at the opening of the follicle, black dots remain. "Favus" is caused by "T. schoenleinii", and is endemic in South Africa and the Middle East. It is characterized by a number of yellowish, circular, cup-shaped crusts (scutula) grouped in patches like a piece of honeycomb, each about the size of a split pea, with a hair projecting in the center. These increase in size and become crusted over, so that the characteristic lesion can only be seen around the edge of the scab.

Unlike most other manifestations of Tinea dermatophyte infections, Kerion is not sufficiently treated with topical antifungals and requires systemic therapy. Typical therapy consists of oral antifungals, such as griseofulvin or terbinafine, for a sustained duration of at least 6-8 weeks depending on severity. Successful treatment of kerion often requires empiric bacterial antibiotics given the high prevalence of secondary bacterial infection.

The bacteria staphylococci are present in the majority of cases. Treatment with systemic antibiotics and coal tar shampoo can completely clear the condition when Staphylococcus aureus bacteria are found. Fungal infections such as tinea capitis are known to mimic the symptoms of the condition and can be cleared with antifungal treatment.

A dermatomycosis is a skin disease caused by a fungus. This excludes dermatophytosis.

Examples of dermatomycoses are tinea and cutaneous candidiasis.

Kerion is the result of the host's response to a fungal ringworm infection of the hair follicles of the scalp (occasionally the beard) that can be accompanied by secondary bacterial infection(s). It usually appears as raised, spongy lesions, and typically occurs in children. This honeycomb is a painful inflammatory reaction with deep suppurative lesions on the scalp. Follicles may be seen discharging pus. There may be sinus formation and rarely mycetoma-like grains are produced. It is usually caused by dermatophytes (fungal infections of the skin affecting humans and animals) such as "Trichophyton verrucosum", "T. mentagrophytes", and "Microsporum canis". Treatment with oral griseofulvin common.

Genetic, environmental, hormonal, and immune-system factors have been shown to be involved in the manifestation of seborrhoeic dermatitis.

Seborrhoeic dermatitis may be aggravated by illness, psychological stress, fatigue, sleep deprivation, change of season and reduced general health.

In children, excessive vitamin A intake can cause seborrhoeic dermatitis. Lack of biotin, pyridoxine (vitamin B), or riboflavin (vitamin B) may be a cause in babies.

Those with immunodeficiency (especially infection with HIV) and with neurological disorders such as Parkinson's disease (for which the condition is an autonomic sign) and stroke are particularly prone to it.

According to a 2016 study, bacteria (mainly Propionibacterium and Staphylococcus) are more important to dandruff formation than fungi. Bacterial presence was in turn influenced by water and sebum amount.

Older literature cites the fungus "Malassezia furfur" (previously known as "Pityrosporum ovale") as the cause of dandruff. While this species does occur naturally on the skin surface of both healthy people and those with dandruff, in 2007 it was discovered that the responsible agent is a scalp specific fungus, "Malassezia globosa", that metabolizes triglycerides present in sebum by the expression of lipase, resulting in a lipid byproduct oleic acid. During dandruff, the levels of "Malassezia" increase by 1.5 to 2 times its normal level. Oleic acid penetrates the top layer of the epidermis, the stratum corneum, and evokes an inflammatory response in susceptible people which disturbs homeostasis and results in erratic cleavage of stratum corneum cells.

Pityriasis amiantacea (also known as "Tinea amiantacea") is an eczematous condition of the scalp in which thick tenaciously adherent scale infiltrates and surrounds the base of a group of scalp hairs. It does not result in scarring or alopecia.

Pityriasis amiantacea was first described by Alibert in 1832. Pityriasis amiantacea affects the scalp as shiny asbestos-like (amiantaceus) thick scales attached in layers to the hair shaft. The scales surround and bind down tufts of hair. The condition can be localised or covering over the entire scalp. Temporary alopecia and scarring alopecia may occur due to repeated removal of hairs attached to the scale. It is a rare disease with a female predilection.

Pityriasis amiantacea can easily be misdiagnosed due its close resemblance to other scalp diseases such as psoriasis, seborrhoeic dermatitis or lichen planus. However in pityriasis amiantacea the scales are attached to both the hair shaft and the scalp. Pityriasis amiantacea may be present with other inflammatory conditions such as atopic dermatitis or seborrhoeic dermatitis and sebaceous scales and alopecia can occur. According to the dermatology text Bolognia this condition is most often seen in psoriasis, but may also be seen in secondarily infected atopic dermatitis, seborrheic dermatitis, and tinea capitis.

If the condition thickens, turns red and irritated, starts spreading, appears on other body parts, or if the baby develops thrush (fungal mouth infection), fungal ear infection (an ear infection that does not respond to antibiotics) or a persistent diaper rash, medical intervention is recommended.

Severe cases of cradle cap, especially with cracked or bleeding skin, can provide a place for bacteria to grow. If the cradle cap is caused by a fungal infection which has worsened significantly over days or weeks to allow bacterial growth (impetigo, most commonly), a combination treatment of antibiotics and antifungals may be necessary. Since it is difficult for a layperson to distinguish the difference between sebaceous gland cradle cap, fungal cradle cap, or either of these combined with a bacterial infection, medical advice should be sought if the condition appears to worsen.

Cradle cap is occasionally linked to immune disorders. If the baby is not thriving and has other problems (e.g. diarrhea), a doctor should be consulted.

Dandruff can have several causes, including dry skin, seborrhoeic dermatitis, not cleaning/scrubbing often enough, shampooing too often, psoriasis, eczema, sensitivity to hair care products, or a yeast-like fungus. Dry skin is the most common cause of flaking dandruff.

As the skin layers continually replaces itself, cells are pushed outward where they die and flake off. For most individuals, these flakes of skin are too small to be visible. However, certain conditions cause cell turnover to be unusually rapid, especially in the scalp. It is hypothesized that for people with dandruff, skin cells may mature and be shed in 2–7 days, as opposed to around a month in people without dandruff. The result is that dead skin cells are shed in large, oily clumps, which appear as white or grayish flakes on the scalp, skin and clothes.

According to one study, dandruff has been shown to be possibly the result of three factors:

1. Skin oil commonly referred to as sebum or sebaceous secretions

2. The metabolic by-products of skin micro-organisms (most specifically Malassezia yeasts)

3. Individual susceptibility and allergy sensitivity.

Seborrhoeic dermatitis may involve an inflammatory reaction to a proliferation of a form of the yeast "Malassezia", though this has not been proven.

The main species of yeast found on the scalp of those with the condition is "Malassezia globosa", others being "Malassezia furfur" (formerly known as "Pityrosporum ovale") and "Malassezia restricta". It has been suggested that the yeast produces toxic substances that irritate and inflame the skin. Patients with seborrhoeic dermatitis appear to have a reduced resistance to the yeast. However, the colonization rate of affected skin may be lower than that of unaffected skin.

Only saturated fatty acids (FAs) have been shown to support "Malassezia" growth. It has also been shown that while number density of "M. globosa" and "M. restricta" do not directly correlate to dandruff presence or severity, removal correlates directly with amelioration of flaking. Furthermore, in dandruff-susceptible individuals pure oleic acid, an unsaturated FA and "Malassezia" metabolite, induces flaking in the absence of "Malassezia" by direct effects on the host skin barrier. These findings support the following hypothesis:

"Malassezia" hydrolyze human sebum, releasing a mixture of saturated and unsaturated fatty acids. They take up the required saturated FAs, leaving behind unsaturated FAs. The unsaturated FAs penetrate the stratum corneum. Because of their non-uniform structure, they breach the skin's barrier function. This barrier breach induces an irritation response, leading to dandruff and seborrhoeic dermatitis.

Assurances that this condition will clear as the baby matures are very common. However, studies have shown that the condition occasionally persists into the toddler years, and less commonly into later childhood. It tends to recur in adolescence and persists into adulthood. In an Australian study, about 15 percent of previously diagnosed children still had eczema 10 years later. Sometimes, cradle cap turns into atopic dermatitis. Rarely, it turns out to be misdiagnosed psoriasis.

Acne keloidalis nuchae (also known as "Acne keloidalis", "Dermatitis papillaris capillitii", "Folliculitis keloidalis", "Folliculitis keloidis nuchae", and "Nuchal keloid acne") is a destructive scarring folliculitis that occurs almost exclusively on the occipital scalp of people of African descent, primarily men. This is mainly because men often cut their hair very low as opposed to women, allowing the hair to prick the occipital scalp and upset it. Acne keloidalis nuchae most commonly presents itself in individuals aged 13 to 25. The disease is closely related to pseudofolliculitis barbae and both occur frequently in black men in the military, where it is so common that services often have widely known protocols for management.

With no particular affinity to any particular ethnic group, seen in all age groups and equally amongst males and females, the precise prevalence is not known.

Keratoderma blennorrhagicum etymologically meaning keratinized (kerato-) skin (derma-) mucousy (blenno-) discharge (-rrhagia) (also called keratoderma blennorrhagica) are skin lesions commonly found on the palms and soles but which may spread to the scrotum, scalp and trunk. The lesions may resemble psoriasis.

Keratoderma blennorrhagicum is commonly seen as an additional feature of reactive arthritis in almost 15% of male patients. The appearance is usually of a vesico-pustular waxy lesion with a yellow brown colour. These lesions may join together to form larger crusty plaques with desquamating edges.

The cat must have a supply of niacin, as cats cannot convert tryptophan into niacin like dogs. However, diets high in corn and low in protein can result in skin lesions and scaly, dry, greasy skin, with hair loss. Another B vitamin, biotin, if deficient causes hair loss around the eyes and face. A lack of B vitamins can be corrected by supplementing with a vitamin B complex, and brewers yeast.

The most important infectious skin diseases of cats is ringworm or dermatophytosis. Other cat skin infections include parasitic diseases like mange and lice infestation.

Other ectoparasites, including flea and tick infestations are not considered directly contagious but are acquired from an environment where other infested hosts have established the parasite's life cycle.

Another common skin infection is cat bite abscess. A mixture of bacteria introduced by a bite wound cause infections in pockets under the skin and affected cats often show manic depression and fever.

Other rashes that occur in a widespread distribution can look like an id reaction. These include atopic dermatitis, contact dermatitis, dyshidrosis, photodermatitis, scabies and drug eruptions.